SUMMARY:The purpose of this study was to investigate the ultrastructural effects of lead on the kidney cortex of rats. Wistar Albino rats (180-200g body weight) were divided into a controlled and lead acetate-exposed group. Rats received lead acetate at 500 ppm in their drinking water for 60 days. Both groups were fed with the same standard food, but lead acetate was added to the drinking water. During the experimental period, blood samples were taken from the abdominal aorta of the anesthetised animals. At the end of exposure, body weight and blood lead levels were measured. The kidney tissue samples were prepared and analyzed by light and transmission electron microscopy. Cortical renal tubules show various degenerative changes with focal tubular necrosis invaded by inflammatory cells. The ultrastructural alterations found in lead acetate-treated rats were a diminution in the amount of filtration slits, increased fusion of foot processes in epithelial cells of the glomeruli, increase of lysosomal structures and pinocytic vesicles as well as large mitochondria in proximal tubule cells.

SUMMARY:Formaldehyde inhalation, are known to be nasal mucosa irritating feature. This study we are examined the effects histopathologic of formaldehyde inhalation on rats by using light microscopy. 16 adult wistar albino rats were used in this study. 8 rats were in control group and 8 rats were in experiment group. Experiment group was exposed to 10 ppm formaldhyde 8hours/day,5days/ week for 8 week. Nasal mucosa was removed and placed in 10% formaline. Sections were stained with Hematoxylene-Eosine and observed under light microscopy. The lining epithelium of respiratory mucosa showed a loss of ciliated cells with metaplasia of goblet cells and hyperplasia of squamous cells.

ObjectiveTraumatic brain injury causes tissue damage, breakdown of cerebral blood flow and metabolic regulation. This study aims to investigate the protective influence of antioxidant Ganoderma lucidum (G. lucidum) polysaccharides (GLPs) on brain injury in brain-traumatized rats.MethodsSprague-Dawley conducted a head-traumatized method on rats by dropping off 300 g weight from 1 m height. Groups were categorized as control, G. lucidum, trauma, trauma+ G. lucidum (20 mL/kg per day via gastric gavage). Brain tissues were dissected from anesthetized rats 7 days after injury. For biochemical analysis, malondialdehyde, glutathione and myeloperoxidase values were measured.ResultsIn histopathological examination, neuronal damage in brain cortex and changes in blood brain barrier were observed. In the analysis of immunohistochemical and western blot, p38 mitogen-activated protein kinase, vascular endothelial growth factor and cluster of differentiation 68 expression levels were shown. These analyzes demonstrated the beneficial effects of GLPs on brain injury.ConclusionWe propose that GLPs treatment after brain injury could be an alternative treatment to decraseing inflammation and edema, preventing neuronal and glial cells degeneration if given in appropriate dosage and in particular time intervals.

Traumatic brain injury (TBI) can potentially lead to hemorrhages in all areas of the skull, which can damage cells and nerve connections. This study aims to investigate the protective effects of Ganoderma lucidum polysaccharides (GLPS) as a antioxidant on cerebellar cell tissues after traumatic brain injury in rats. Sprague Dawley rats were subjected to TBI with a weight-drop device using 300 g-1m weight-height impact. The groups are consisted of control, trauma, and trauma+Ganoderma lucidum groups. At seven days post-brain injury, experimental rats were decapitated after intraperitoneal administration of ketamine HCL (0.15 ml/100 g body weight). Cereballar samples were taken for histological examination or determination of malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) activity. Significant improvement was observed in cells and vascular structures of Ganoderma lucidum treated groups when compared to untreated groups. It is believed that Ganoderma lucidum may have an effect on the progression of traumatic brain injury. Ganoderma lucidum application may affect angiogenetic development in blood vessel endothelial cells, decrease inflammatory cell accumulation by affecting cytokine mechanism and may create apoptotic nerve cells and neuroprotective mechanism in glial cells.

SUMMARY: Cadmium Chloride (CdC1) is a teratogen which is commonly used in industry. Although it is well known to cause toxicity in testes, kidney, heart and liver, few studies have been carried out in the digestive system. In the present study the effects of CdC1 on the esophagus of rats were investigated Wistar albino rats weighing 180 -200 g were used. The animals were divided into two groups; one group was administered 2 mg/kg/day CdC1 intraperitoneally for one week. Esophagus was removed and placed in 10% formaline. Sections were stained with Hematoxylene-Eosine and observed under light microscopy. Hyperplasia in the epithelium, an increase in fibrotic cells under epithelium, hemorrhage in vessels, free floating erythrocytes were all observed following fetal exposure. In conclusion and most importantly, cadmium chloride was found to cause an increase in connective tissue in esophagus mucosa.